Influence of zinc on the normal and ischaemic retina

In the mammalian retina, endogenous chelatable zinc§was shown to be localised mainly in the§photoreceptors and retinal pigment epithelium. Zinc§localisation in the photoreceptors varied in light§and dark. Low (100 micromolar) levels of zinc§sulphate (ZnSO4) counteracted glutamate- and§NMDA-induced lactate dehydrogenase release in rat§cortical cultures; as well as the changes in§Gamma-aminobutyric acid (GABA)-immunoreactivity§mediated by experimental ischaemia and NMDA in§isolated rabbit retinas. However, high (500§micromolar) levels of ZnSO4 caused lactate§dehydrogenase release and alterations in§GABA-immunoreactivity, and exacerbated the effects of§NMDA or ischaemia to the retina. When very low (1§micromolar) concentrations of ZnSO4 were present§during ischaemia, GABA-immunoreactivity was localised§to Müller cells, indicating that zinc prevents the§metabolism of GABA in Müller cells in the ischaemic§retina. High (500 micromolar) concentrations of ZnSO4§potentiated reactive oxygen species formation while§ameliorating lipid peroxidation. When low (1 nanomol)§levels of ZnSO4 were injected into the vitreous§humour of the rabbit eye the retina remained unaffected.